RT Journal Article
SR Electronic
T1 Phorbol ester-mediated inhibition of vasopressin and beta-adrenergic responses in a vascular smooth muscle cell line.
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 180
OP 184
VO 31
IS 2
A1 N Aiyar
A1 P Nambi
A1 M Whitman
A1 F L Stassen
A1 S T Crooke
YR 1987
UL http://molpharm.aspetjournals.org/content/31/2/180.abstract
AB We have reported previously that in the vascular smooth muscle cell line A-10 (ATCC CRL 1476), vasopressin stimulated phosphatidylinositol turnover Ca2+ efflux and inhibited isoproterenol-stimulated cAMP accumulation. Here we report that pretreatment of these cells with phorbol dibutyrate, an activator of protein kinase C, attenuated the responses to vasopressin and isoproterenol. This effect was concentration dependent and could be observed after pretreatment for 2 min. 4 alpha Phorbol 12,13-didecanoate, which does not activate protein kinase C, did not attenuate the responses. These data suggest that activation of protein kinase C by phorbol dibutyrate attenuates the responses of vascular smooth muscle cells to isoproterenol and vasopressin. Although phorbol ester did not affect [3H]-8-arginine vasopressin binding to intact cells, it appeared to uncouple vasopressin receptors from guanine nucleotide-binding protein.